Associative memory neurons of encoding multi-modal signals are recruited by neuroligin-3-mediated new synapse formation.

The joint storage and reciprocal retrieval of learnt associated signals are presumably encoded by associative memory cells. In the accumulation and enrichment of memory contents in lifespan, a signal often becomes a core signal associatively shared for other signals. One specific group of associative memory neurons that encode this core signal likely interconnects multiple groups of associative memory neurons that encode these other signals for their joint storage and reciprocal retrieval. We have examined this hypothesis in a mouse model of associative learning by pairing the whisker tactile signal sequentially with the olfactory signal, the gustatory signal, and the tail-heating signal. Mice experienced this associative learning show the whisker fluctuation induced by olfactory, gustatory, and tail-heating signals, or the other way around, that is, memories to multi-modal associated signals featured by their reciprocal retrievals. Barrel cortical neurons in these mice become able to encode olfactory, gustatory, and tail-heating signals alongside the whisker signal. Barrel cortical neurons interconnect piriform, S1-Tr, and gustatory cortical neurons. With the barrel cortex as the hub, the indirect activation occurs among piriform, gustatory, and S1-Tr cortices for the second-order associative memory. These associative memory neurons recruited to encode multi-modal signals in the barrel cortex for associative memory are downregulated by neuroligin-3 knockdown. Thus, associative memory neurons can be recruited as the core cellular substrate to memorize multiple associated signals for the first-order and the second-order of associative memories by neuroligin-3-mediated synapse formation, which constitutes neuronal substrates of cognitive activities in the field of memoriology.

The Dof transcription factor COG1 acts as a key regulator of plant biomass by promoting photosynthesis and starch accumulation.

Photosynthetic efficiency is the primary determinant of crop yield, including vegetative biomass and grain yield. Manipulation of key transcription factors known to directly control photosynthetic machinery can be an effective strategy to improve photosynthetic traits. In this study, we identified an Arabidopsis gain-of-function mutant, cogwheel1-3D, that shows a significantly enlarged rosette and increased biomass compared with wild-type plants. Overexpression of COG1, a Dof transcription factor, recapitulated the phenotype of cogwheel1-3D, whereas knocking out COG1 and its six paralogs resulted in a reduced rosette size and decreased biomass. Transcriptomic and quantitative reverse transcription polymerase chain reaction analyses demonstrated that COG1 and its paralogs were required for light-induced expression of genes involved in photosynthesis. Further chromatin immunoprecipitation and electrophoretic mobility shift assays indicated that COG1 can directly bind to the promoter regions of multiple genes encoding light-harvesting antenna proteins. Physiological, biochemical, and microscopy analyses revealed that COG1 enhances photosynthetic capacity and starch accumulation in Arabidopsis rosette leaves. Furthermore, combined results of bioinformatic, genetic, and molecular experiments suggested that the functions of COG1 in increasing biomass are conserved in different plant species. These results collectively demonstrated that COG1 acts as a key regulator of plant biomass by promoting photosynthesis and starch accumulation. Manipulating COG1 to optimize photosynthetic capacity would create new strategies for future crop yield improvement.